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INTRODUCTION: There are many reasons to believe that the nitric oxide/guanosine 3'5' - cyclic monophosphate (or NO/cGMP) pathway on vasoplegic states is underestimated. To study indigo carmine (IC) as an alternative to methylene blue was the investigation rationale. METHODS: The IC (3mg/kg intravenous infusion) study protocol included five experimental groups; 1) Control group - saline was injected at 0 and 10 minutes; 2) IC group - IC was injected at 0 and saline at 10 minutes; 3) compound 48/80 (C48/80) group - C48/80 was injected at 0 minute and saline at 10 minutes; 4) C48/80 + IC group - C48/80 was injected at 0 minute and IC at 10 minutes; and 5) IC + C48/80 group - IC was injected at 0 minute and C48/80 at 10 minutes. The studies were carried out by registering and measuring hemodynamic and blood gasometric parameters, including continuous cardiac output. RESULTS: 1) The effects of the drugs (IC and C48/80) were more evident in the first 20 minutes of recording; 2) hypotensive responses were more pronounced in the C48/80 groups; 3) IC isolated or applied before C48/80 caused transient pulmonary hypertension; and 4) after the first 20 minutes, the pressure responses showed stability with apparent hypotension more pronounced in the C48/80 groups. Clinical observations showed significant hemodynamic instability and catastrophic anaphylactic reactions (agitation, pulmonary hypertension, severe bronchospasm, urticaria, high-intensity cyanosis, violent gastric hypersecretion, and ascites). CONCLUSION: A global results analysis showed differences between groups only in the first 20 minutes of the experiments.

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Abstract Introduction: There are many reasons to believe that the nitric oxide/guanosine 3'5' - cyclic monophosphate (or NO/cGMP) pathway on vasoplegic states is underestimated. To study indigo carmine (IC) as an alternative to methylene blue was the investigation rationale. Methods: The IC (3mg/kg intravenous infusion) study protocol included five experimental groups; 1) Control group — saline was injected at 0 and 10 minutes; 2) IC group — IC was injected at 0 and saline at 10 minutes; 3) compound 48/80 (C48/80) group — C48/80 was injected at 0 minute and saline at 10 minutes; 4) C48/80 + IC group — C48/80 was injected at 0 minute and IC at 10 minutes; and 5) IC + C48/80 group — IC was injected at 0 minute and C48/80 at 10 minutes. The studies were carried out by registering and measuring hemodynamic and blood gasometric parameters, including continuous cardiac output. Results: 1) The effects of the drugs (IC and C48/80) were more evident in the first 20 minutes of recording; 2) hypotensive responses were more pronounced in the C48/80 groups; 3) IC isolated or applied before C48/80 caused transient pulmonary hypertension; and 4) after the first 20 minutes, the pressure responses showed stability with apparent hypotension more pronounced in the C48/80 groups. Clinical observations showed significant hemodynamic instability and catastrophic anaphylactic reactions (agitation, pulmonary hypertension, severe bronchospasm, urticaria, high-intensity cyanosis, violent gastric hypersecretion, and ascites). Conclusion: A global results analysis showed differences between groups only in the first 20 minutes of the experiments.

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Although hypothermia has received substantial attention as an indicator of severity in anaphylaxis, it has been neglected from the perspective of whether it could act as a disease-modifying factor in this condition. Here, the impact of naturally occurring (spontaneous) hypothermia on anaphylaxis was evaluated in a murine model of ovalbumin (OVA)-induced allergy. Nonextreme changes in the ambient temperature (Ta) were used to modulate the magnitude of spontaneous hypothermia. At a Ta of 24°C, challenge with OVA intraperitoneally or intravenously resulted in a rapid, transient fall in body core temperature, which reached its nadir 4-6°C below baseline in 30 min. This hypothermic response was largely attenuated when the mice were kept at a Ta of 34°C. The Ta-dependent attenuation of hypothermia resulted in a survival rate of only 30%, as opposed to survival of 100% in the condition that favored the development of hypothermia. The protective effect of hypothermia did not involve changes in the rate of mast cell degranulation, as assessed by the concentration of mast cell protease-1 in bodily fluids. On the other hand, hypothermia improved oxygenation of the brain and kidneys, as indicated by higher NAD+/NADH ratios. Therefore, it is plausible to propose that naturally occurring hypothermia makes organs more resistant to the anaphylactic insult.

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Anaphylaxis is a life-threatening clinical condition that results from the activation of mast cells/basophils, inflammatory pathways, or both. It can be specific (allergic), or non-specific (non-allergic). Most anaphylaxis are mediated by IgE, but there are also some mediated by IgM and complement activation. Incidence is about 1:10,000 anesthesia. Recent studies show that the drugs or substances mostly implicated in producing perioperative anaphylaxis are: neuromuscular blockers (60.6%), antibiotics (18.2%), patent blue dye (5.4%) and latex (5.2%). However, all drugs and substances used during anesthesia and surgery, perhaps with the sole exception of inhalation agents and crystalloids, have been reported as potentially causes of anaphylaxis. The clinical presentation is multisystemic, producing signs and symptoms mainly on skin, respiratory, cardiovascular, gastrointestinal and central nervous systems. In its advanced phase, it may evolve to anaphylactic shock, causing tissue hypoperfusion and leading to altered cell integrity and multiple organ failure, associated with high mortality. Diagnosis is based on clinical presentation (history and clinical manifestations), biological evidence (serum tryptase levels, serum histamine levels and search for specific IgE) and allergological evidence (skin tests, provocation test, mediator release tests and tests of activation of basophils). Treatment include 3 stages: general measures, first-line or primary treatment and second-line or secondary treatment. General measures consist of: Trendelenburg position, invasive monitoring (according to the severity of the clinical presentation), 100% oxygen administration, discontinuation of drugs and/or suspected agents and asking for help. The primary treatment is epinephrine in doses proportional to the clinical manifestations, airway support, 100% oxygen and aggressive resuscitation with intravenous fluids. Secondary treatment includesadministration of bronchialodilators, corticosteroids, and antihistamines.

Una anafilaxia es una condición clínica potencialmente mortal que resulta de la activación específica (alérgica), o no específica (no alérgica) de mastocitos/ basófilos, vías inflamatorias o ambos. La mayoría de las anafilaxias son mediadas por IgE, pero también las hay por IgM y activación del complemento. Su incidencia es de 1:10.000 anestesias. En los últimos estudios, los fármacos o sustancias más implicadas en producir anafilaxia perioperatoria son los bloqueadores neuromusculares (60,6%), los antibióticos (18,2%), las tinturas azules (5,4%) y el látex (5,2%), sin embargo, todas las drogas y sustancias usadas durante la anestesia y la cirugía, tal vez con la única excepción de los agentes inhalatorios y los cristaloides, han sido reportadas como potencialmente causantes de anafilaxia. El cuadro clínico es multisistémico, originando signos y síntomas centrados en la piel y los sistemas respiratorio, cardiovascular, gastrointestinal y nervioso central. En su fase avanzada puede evolucionar a anafiláctico, causando hipoperfusión tisular y llevando a alteración en la integridad celular y falla de múltiples órganos, con alta mortalidad asociada. El diagnóstico se basa en evidencias clínicas (historia y manifestaciones clínicas), evidencias biológicas (niveles de triptasa sérica, de histamina sérica y búsqueda de IgE específicas) y evidencias alergológicas (pruebas cutáneas, test de provocación, pruebas de liberación de mediadores y pruebas de activación de basófilos. El tratamiento incluye 3 etapas: medidas generales, tratamiento de primera línea o primario y tratamiento de segunda línea o secundario. Las medidas generales consisten en poner al paciente en posición de Trendelemburg, iniciar monitorización invasiva según la intensidad del cuadro clínico, administración de oxígeno al 100%, discontinuación de drogas y/o agentes posiblemente incriminados y pedir ayuda. El tratamiento primario es la adrenalina, en dosis proporcionales a las manifestaciones clínicas, el soporte de la vía aérea manteniendo el oxígeno ql 100% y la reanimación agresiva con fluidos endovenosos. El tratamiento secundario incluye la administración de broncodilatadores, corticoesteroides y antihistamínicos.

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Mastocytosis consists of a heterogeneous group of disorders characterized by an abnormal increase of mast cell in one or more organs or tissues. The degranulation of mast cells with subsequent clinical symptoms can be triggered by psychological, chemical or traumatic agents. The main challenge of these patients is to avoid these triggers in order to prevent an anaphylactic shock. We report a case of a patient diagnosed with cutaneous mastocytoses who underwent urgent appendicectomy. Their perioperative management involves a multidisciniplinary approach. We report the anaesthetic management in this disease.

Las mastocitosis son un grupo heterogéneo de enfermedades que se caracterizan por la proliferación de mastocitos y su posterior acumulación. La degranulación de los mastocitos puede desencadenarse por diferentes agentes como la cirugía, el estrés o los fármacos histaminoliberadores. El principal reto que plantea a un anestesiólogo un paciente con mastocitosis es la posibilidad de que se desencadene una reacción anafiláctica. Se describe el manejo anestésico de un paciente con mastocitosis cutánea. El desconocimiento de esta entidad puede suponer un aumento de la morbimortalidad de estos pacientes.

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Introdução: a anafilaxia é uma reação alérgica sistêmica grave, de início rápido e potencialmente fatal. A despeito da gravidade e da intensidade das reações anafiláticas, os sinais e sintomas desta síndrome são subestimados e não são reconhecidos por pacientes e por médicos. Objetivo: revisar os aspectos principais da epidemiologia, diagnóstico e tratamento da anafilaxia em sala de emergências. Metodologia: foi realizada busca de estudos publicados na língua inglesa, nas bases de dados PUBMED/ MEDLINE que discorressem sobre o tema anafilaxia. Os estudos foram selecionados após a definição dos DeCS e MeSH: alergia, hipersensibilidade, choque anafilático, emergência e morte. Estes termos foram cruzados por meio do chaveador boleano (AND). Os dados foram coletados no período de maio de 2017 a agosto de 2017. Conclusão: a anafilaxia caracteriza-se por ser uma síndrome sistêmica, multiorgânica, potencialmente fatal porem ainda de difícil diagnóstico. Epinefrina constitui-se o tratamento de escolha na emergência.

Introduction: anaphylaxis is a serious, early-onset and potentially fatal systemic allergic reaction. Despite the severity and intensity of anaphylactic reactions, the signs and symptoms of this syndrome are underestimated and are not recognized by patients and physicians. Objective: to review the main aspects of epidemiology, diagnosis and treatment of anaphylaxis in an emergency room. Methodology: a search was made for studies published in the English language, in PUBMED / MEDLINE databases that discuss the topic of anaphylaxis. The studies were selected after the definition of DeCS and MeSH: allergy, hypersensitivity, anaphylactic shock, emergency and death. These terms were crossed by the boolean switch (AND). The data were collected from May 2017 to August 2017. Conclusion: anaphylaxis is characterized by a systemic, multiorganic syndrome, potentially fatal but difficult to diagnose. Epinephrine is the treatment of choice in the emergency room.

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Cystic echinococcosis (CE) is an anthropozoonotic disease with worldwide distribution and is caused by the cestode Echinococcus granulosus. Anaphylactic shock induced by CE rupture is a serious complication especially in patients with hydatid infections, as the resulting leakage of fluid contains highly toxic endogenous antigen. We aimed to isolate and identify the antigens of specific IgE and IgG1 (sIgE and sIgG1) in E. granulosus cyst fluid (EgCF). Crude antigen for EgCF was prepared from E. granulosus-infected sheep liver. Antigens were separated and identified by one-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis (1D SDS-PAGE), two-dimensional gel electrophoresis (2-DE), and immunoblotting. Results of 1D SDS-PAGE and immunoblotting showed that 40.5 kDa protein was the major antigen of sIgE, and 35.5 kDa protein was the major antigen of sIgG1 in EgCF. Results of 2-DE and immunoblotting showed that main antigens of sIgE in EgCF were four proteins with pI values ranging from 6.5 to 9.0 and a molecular weight of 40.5 kDa. Main antigens of sIgG1 in EgCF were five proteins with pI values ranging from 6.5 to 9.0 and a molecular weight of 35.5 kDa. The antigens identified for sIgE and sIgG1 can provide critical insights into cellular and molecular mechanisms underlying anaphylactic shock induced by CE.

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RESUMEN Objetivo: exponer dos casos clínicos de pacientes que presentaron una reacción anafiláctica grave durante la anestesia con diferente evolución clínica. Caso 1: sexo femenino, 19 años, coordinada para resección de quiste tirogloso. Niega antecedentes de alergia. Durante inducción anestésica presenta taquicardia e hipotensión arterial severa, con exantema cutáneo. Se trató con cristaloides, adrenalina, hidrocortisona y clorfeniramina intravenosas, recuperando la estabilidad hemodinámica rápidamente, suspendiéndose el procedimiento. Postoperatorio: test cutáneo positivo para atracurio. Caso 2: Sexo femenino, 57 años, coordinada para sustitución valvular aórtica por estenosis severa sintomática. Cesárea hace 25 años, en la cual durante la inducción anestésica presentó reacción anafiláctica grave con paro cardiorrespiratorio. Cateterismo cardíaco hace 1 mes, sin incidentes, tres días antes se realizó corticoides vía oral. La noche previa a la sustitución valvular se administró corticoides y antihistamínicos vía oral. Alérgica a dipirona, ácido acetilsalicílico (AAS), ampicilina, cefradina, yodo y “drogas anestésicas”. Durante inducción anestésica presenta shock anafiláctico con hipotensión severa refractaria a, tratamiento de reanimación, falleciendo en block quirúrgico. Discusión: la incidencia de las reacciones anafilácticas varía desde 1/3.500 a 1/20.000 anestesias, con una mortalidad perioperatoria entre 3% y 10%, presentándose cerca de 90% durante la inducción anestésica. Los relajantes musculares son los fármacos más involucrados. El manejo específico y temprano en cada una de las etapas mejora los resultados. La única medida eficaz para prevenir una reacción anafiláctica es evitar el contacto con el agente responsable. Conclusiones: se presentan casos clínicos en los que la preparación y el tratamiento pudo incidir en la evolución de los pacientes.

SUMMARY Objective: to present two clinical cases of patients who had a severe anaphylactic reaction during anesthesia with a different clinical evolution. Case 1: female, 19 years of age, with scheduled surgery for thyroglossal cyst removal. No history of allergy. During induction of anesthesia she presented tachycardia and severe hypotension, with skin exanthema. Treatment administered: intravenous, Adrenaline, Hydrocortisone, Chlorpheniramine and crystalloids, which resulted in a rapid restoration of the hemodynamic stability and the subsequent suspension of the procedure. Postoperative period: atracurium-positive skin test. Case 2: female, 57 years of age, with scheduled surgery for aortic valve replacement due to symptomatic severe stenosis. During anesthetic induction for cesarean section 25 years ago the patient developed serious anaphylactic reaction with cardiorespiratory arrest. Cardiac catheterization 1 month ago with no incidents, oral corticosteroids were administered 3 days before. Oral corticosteroids and antihistamines were administered the night before valve replacement. Allergic to dipyrone, aspirin, ampicillin, cephradine, iodine and "anesthetic drugs". During induction of anesthesia she developed anaphylactic shock with severe refractory hypotension despite resuscitation attempts and died in the operating room. Discussion: incidence of anaphylactic reactions varies from 1/3.500 to 1/20.000 anesthesias, with a perioperative mortality rate between 3 and 10%; around 90% happens during induction of anesthesia. Muscle Relaxants are the mostly involved. Specific and early management in each stage improves the outcomes. The only effective measure to prevent anaphylactic reactions is to avoid contact with the responsible agent. Conclusions: clinical cases are presented in which the preparation and treatment had an effect on patients progress.

RESUMO Objetivo: expor dois casos clínicos de pacientes que apresentaram uma reação anafilática grave durante a anestesia com diferente evolução clinica. Caso 1: paciente do sexo feminino, 19 anos, marcada para cirurgia de cisto tiroglosso. Nega antecedentes de alergia. Durante a indução anestésica apresentou taquicardia e hipotensão arterial severa com exantema cutâneo. O tratamento estabelecido foi: cristalóide, adrenalina, hidrocortisona e clorfeniramina endovenosa, rapidamente restaurou a estabilidade hemodinâmica, suspendendo-se o procedimento. Pós-operatório: teste cutâneo positivo para atracurio. Caso 2: paciente do sexo feminino, 57 anos, marcada para cirurgia de substituição valvular aórtica por estenose severa sintomática. Cesariana há 25 anos, na qual na indução anestésica apresentou reação anafilática grave com parada cardiorrespiratória. Cateterismo cardíaco há 1 mês, sem incidentes, 3 dias antes foi realizado corticóide via oral. Na noite anterior da substituição valvular administrou-se corticóide e anti-histamínico via oral. Alérgica a dipirona, AAS, ampicilina, cefradina, yodo e "drogas anestésicas". Durante a indução anestésica apresentou choque anafilático com hipotensão severa que não respondeu ao tratamento de reanimação, indo a óbito no bloco cirúrgico. Discussão: a incidência das reações anafiláticas é variável, 1/3.500 a 1/20.000 anestesias, com uma mortalidade perioperatoria entre 3 e 10 %, apresentando-se perto do 90 % durante a indução anestésica. Os relaxantes musculares são os maiores responsáveis. A conduta especifica em cada uma das etapas melhora os resultados. A única medida eficaz para prevenir uma reação anafilática é evitar o contato com os agentes responsáveis. Conclusões: apresentam-se casos clínicos nos quais a preparação e tratamento poderia ter efeito sobre a evolução dos pacientes.

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Menos del 5% de las 20.000 especies estimadas de abejas son sociales y, por lo tanto, pueden producirse ataques masivos o generarse situaciones de riesgo al enjambrar o construir panalescerca o en el interior de domicilios. El veneno de abejas está constituido por una mezcla de substancias con proteínas, siendo las principales enzimas, péptidos y aminas biogénicas. Estas proteínas poseen acciones farmacológicas y alergénicas capaces de provocar cuadros de envenenamiento en el humano y en animales. Se describe el caso clínico de un agricultor que sufrió picaduras por más de 500 abejas con desenlace fatal. Además, se realiza una breve revisión de la literatura sobre el tema.

Less than 5% of the estimated 20,000 species of bees are social, and therefore massive attacks might occur or situations of risk could be generated when swarming to build hives near or inside homes. Bee venom consists of a mixture of substances, mainly protein enzymes, peptides and biogenic amines, these proteins have pharmacological actions and allergens can induce boxes poisoning in humans and animals. We describe the case of a farmer who suffered more than 500 stings by bees with a fatal outcome. In addition, a brief review of the literature is presented.

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The murine model of OVA-induced immediate allergic reaction was used to evaluate the effectiveness of intraperitoneal sub-acute treatment with the leaf hydroalcoholic extract of Cissampelos sympodialis (AFL) in the anaphylactic shock reaction, IgE production and the background proliferative response. BALB/c mice treated with AFL ranging from 200 to 400 mg/kg/day for 5 days before and during OVA-sensitization strongly reduced the animal death and promoted reduction in total and OVA-specific serum IgE level. Spleen cells from AFL-treated sensitized animals showed a decreased proliferative background response when compared with non-sensitized animals. These results demonstrated that sub-acute intraperitoneal treatment with Cissampelos sympodialis extract has an anti-allergic effect.